HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/1/C170    most recent 00187.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Hu, Z. Articles by Sayeed, M. M. Search for Related Content PubMed PubMed Citation Articles by Hu, Z. Articles by Sayeed, M. M.

GROWTH, DIFFERENTIATION, AND APOPTOSIS

Suppression of mitochondria-dependent neutrophil apoptosis with thermal injury

Departments of ¹Physiology and ²Surgery, and Burn & Shock Trauma Institute, Stritch School of Medicine, Loyola University Medical Center, Maywood, Illinois 60153

Submitted 7 May 2003 ; accepted in final form 8 September 2003

Neutrophil apoptosis is delayed under trauma and/or sepsis conditions. The mechanism for the delay has remained unclear. We hypothesize that modulation of the mitochondrial pathway of apoptosis contributes to the delay in neutrophil apoptosis with burn injury. Rats were subjected to burn injury (30% of total body surface area, 98°C for 10 s) and euthanatized 24 h postinjury. Blood neutrophils from sham and burn-injured rats were isolated by Ficoll gradient centrifugation and cultured for 2 or 8 h. Neutrophil apoptosis was determined by annexin V and propidium iodide (PI) labeling and flow cytometry. Neutrophil mitochondrial morphology was assessed via histochemical staining (MitoTracker GreenFM) and confocal microscopy. Neutrophils from rats with burn injury showed a decreased level of apoptosis compared with sham rat neutrophils at both 2 and 8 h of incubation. In incubated sham rat neutrophils, mitochondria showed a change from normal "tubular" to an "aggregated" morphology. In contrast, cultured neutrophils from burn rats did not exhibit this mitochondrial morphological transition until 8 h of incubation. Compared with sham rat neutrophils, neutrophils from burn rats showed decreased levels of active caspase-9 and -3. Whereas an upregulation of Bcl-xL and a downregulation of Bax seemed to contribute to decreased apoptosis in burn rat neutrophils at 2 h of incubation, the decreased apoptosis at 8 h appeared to be associated with a decrease in Bax and increased phosphorylated Bad. These data suggest that suppression of the mitochondrial pathway plays an essential role in the delay of polymorphonuclear neutrophil apoptosis with burn injury.

burn; rat; polymorphonuclear leukocytes; caspase-3; caspase-9; cytochrome c; Bcl-xL; Bax; Bad; MitoTracker GreenFM; confocal microscopy

This article has been cited by other articles:

				R.-F. Guo, L. Sun, H. Gao, K. X. Shi, D. Rittirsch, V. J. Sarma, F. S. Zetoune, and P. A. Ward In vivo regulation of neutrophil apoptosis by C5a during sepsis J. Leukoc. Biol., December 1, 2006; 80(6): 1575 - 1583. [Abstract] [Full Text] [PDF]

				J. W. Smith, R. L. Gamelli, S. B. Jones, and R. Shankar Immunologic Responses to Critical Injury and Sepsis J Intensive Care Med, May 1, 2006; 21(3): 160 - 172. [Abstract] [PDF]

				Z. Hu and M. M. Sayeed Activation of PI3-kinase/PKB contributes to delay in neutrophil apoptosis after thermal injury Am J Physiol Cell Physiol, May 1, 2005; 288(5): C1171 - C1178. [Abstract] [Full Text] [PDF]